Evidence map›Paper›PMID 23817738›Full record

ArticleInternational journal of oncology2013

Skeletal muscle mitochondrial uncoupling in a murine cancer cachexia model.

A Aria Tzika, Cibely Cristine Fontes-Oliveira, Alexander A Shestov, Caterina Constantinou, Nikolaos Psychogios, Valeria Righi, Dionyssios Mintzopoulos, Silvia Busquets, Francisco J Lopez-Soriano, Sylvain Milot and 4 more

Open access · bronzeAbstract read
In one paragraph

Article in International journal of oncology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 62 papers.

0numbers the graph read from it
0cells of the map it votes in
62citing papers in PubMed
3.0field-weighted citation impact, top 8% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

62 citing papers in PubMed, 94 citations in OpenAlex.

  1. Article
  2. Article
  3. Exploring heterogeneity: a dive into preclinical models of cancer cachexia.American journal of physiology. Cell physiology · 2024
    Review
  4. Article
  5. Article
  6. Mitochondria transcription and cancer.Cell death discovery · 2024
    Review
  7. Article
  8. Review
  9. Review
  10. PGC-1α overexpression is not sufficient to mitigate cancer cachexia in either male or female mice.Applied physiology, nutrition, and metabolism = Physiologie appliquee, nutrition et metabolisme · 2022
    Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Review
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  19. Article
  20. Article

2 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

14 authors at 6 institutions in 3 countries.

A Aria TzikaNMR Surgical Laboratory, Department of Surgery, Massachusetts General Hospital and Shriners Burn Institute, Harvard Medical School, Boston, MA 02114, USA.
Cibely Cristine Fontes-Oliveira
Alexander A Shestov
Caterina Constantinou
Nikolaos Psychogios
Valeria Righi
Dionyssios Mintzopoulos
Silvia Busquets
Francisco J Lopez-Soriano
Sylvain Milot
Francois Lepine
Michael N Mindrinos
Laurence G Rahme
Josep M Argiles
Burn Institute · USUniversitat de Barcelona · ESInstitut National de la Recherche Scientifique · CAMassachusetts General Hospital · USStanford University · USUniversity of Minnesota · US

Funding

Interruption of Signaling-Mediated Bacterial Persistent InfectionsR33AI105902 · NIAID · MASSACHUSETTS GENERAL HOSPITAL · PI RAHME, LAURENCE G · 2015 to 2017
$1.8M
NIAID NIH HHS R33 AI105902
6 · The paper itself

Abstract

Approximately half of all cancer patients present with cachexia, a condition in which disease-associated metabolic changes lead to a severe loss of skeletal muscle mass. Working toward an integrated and mechanistic view of cancer cachexia, we investigated the hypothesis that cancer promotes mitochondrial uncoupling in skeletal muscle. We subjected mice to in vivo phosphorous-31 nuclear magnetic resonance (31P NMR) spectroscopy and subjected murine skeletal muscle samples to gas chromatography/mass spectrometry (GC/MS). The mice used in both experiments were Lewis lung carcinoma models of cancer cachexia. A novel 'fragmented mass isotopomer' approach was used in our dynamic analysis of 13C mass isotopomer data. Our 31P NMR and GC/MS results indicated that the adenosine triphosphate (ATP) synthesis rate and tricarboxylic acid (TCA) cycle flux were reduced by 49% and 22%, respectively, in the cancer-bearing mice (p<0.008; t-test vs. controls). The ratio of ATP synthesis rate to the TCA cycle flux (an index of mitochondrial coupling) was reduced by 32% in the cancer-bearing mice (p=0.036; t-test vs. controls). Genomic analysis revealed aberrant expression levels for key regulatory genes and transmission electron microscopy (TEM) revealed ultrastructural abnormalities in the muscle fiber, consistent with the presence of abnormal, giant mitochondria. Taken together, these data suggest that mitochondrial uncoupling occurs in cancer cachexia and thus point to the mitochondria as a potential pharmaceutical target for the treatment of cachexia. These findings may prove relevant to elucidating the mechanisms underlying skeletal muscle wasting observed in other chronic diseases, as well as in aging.

Indexed as

Citric Acid CycleAdenosine TriphosphateAnimalsCachexiaHumansMagnetic Resonance SpectroscopyMiceMicroscopy, Electron, TransmissionMitochondriaMuscle, SkeletalNeoplasmsAdenosine Triphosphate

Identifiers

PMID23817738
PMCPMC6903904
OpenAlexW2147556188

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

Registered trials

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.